scholarly journals Transcriptional regulation of urokinase (uPA) gene expression in breast cancer cells: Role of DNA methylation.

1999 ◽  
Vol 81 (3) ◽  
pp. 443-450 ◽  
Author(s):  
Rosie H. Xing ◽  
Shafaat A. Rabbani
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Dna Methylation ◽  
Transcriptional Regulation ◽  
Cancer Cells ◽  
Breast Cancer Cells

scholarly journals O-GlcNAc regulates MTA1 transcriptional activity during breast cancer cells genotoxic adaptation

2021 ◽  
Author(s):  
Xueqin Xie ◽  
Qiutong Wu ◽  
Keren Zhang ◽  
Yimin Liu ◽  
Nana Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Transcriptional Regulation ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Genotoxic Stress ◽  
Histone Deacetylation ◽  
Nurd Complex ◽  
Nucleosome Remodeling

AbstractChromatin modifier metastasis-associated protein 1 (MTA1), closely correlated with the development and progression in breast cancer, has a vital role in multiple cellular processes, including gene expression and cell homeostasis. Although MTA1 is a stress-responsive gene, its role in genotoxic adaptation remains unexplored. The current study sought to investigate the role of MTA1 and its O-GlcNAc modification in breast cancer cells genotoxic adaptation by using quantitative proteomics, ChIP-seq, transcriptome analysis, loss-and gain-of-functions experiments. We demonstrate that O-GlcNAc modification promotes MTA1 to interact with chromatin and regulates target gene expression, contributing to breast cancer cell genotoxic adaptation. MTA1 is modified with O-GlcNAc residues at serine 237/241/246 in adriamycin adaptive breast cancer cells and that modification improves the genome-wide interactions of MTA1 with gene promotor regions by enhancing its association with nucleosome remodeling and histone deacetylation (NuRD) complex. Further, O-GlcNAc-modulated MTA1 chromatin-binding influences the specific transcriptional regulation of genes involved in the adaptation of breast cancer cells to genotoxic stress. Our findings reveal a previously unrecognized role of O-GlcNAc MTA1 in transcriptional regulation and suggest that O-GlcNAc modification is a promising therapeutic target to overcome chemoresistance in breast cancers.

scholarly journals Role of DNA methylation in miR-200c/141 cluster silencing in invasive breast cancer cells

2010 ◽  
Vol 3 (1) ◽  
Author(s):  
Rui Neves ◽  
Christina Scheel ◽  
Sandra Weinhold ◽  
Ellen Honisch ◽  
Katharina M Iwaniuk ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Methylation ◽  
Cancer Cells ◽  
Invasive Breast Cancer ◽  
Breast Cancer Cells

scholarly journals Role of specificity protein transcription factors in estrogen-induced gene expression in MCF-7 breast cancer cells

2007 ◽  
Vol 39 (4) ◽  
pp. 289-304 ◽  
Author(s):  
Shaheen Khan ◽  
Fei Wu ◽  
Shengxi Liu ◽  
Qian Wu ◽  
Stephen Safe
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Retinoic Acid Receptor ◽  
Estrogen Receptor Α ◽  
Mrna Levels ◽  
Aspartate Transcarbamylase ◽  
Mcf 7

AbstractDeletion analysis of several 17β-estradiol (E2)-responsive genes have identified GC-rich sites that are associated with hormone-induced transactivation in MCF-7 breast cancer cells. However, the role of individual specificity proteins (Sps) in mediating hormone-induced gene expression has not been unequivocally determined. In transient transfection studies using E2-responsive GC-rich promoters from the E2F1, carbamoylphosphate synthetase/aspartate transcarbamylase/dihydroorotase (CAD), and retinoic acid receptor α (RARα) genes, RNA interference using small inhibitory RNAs for Sp1 (iSp1), Sp3 (iSp3), and Sp4 (iSp4) decreased both basal and E2-induced transactivation. The contributions of individual Sp proteins to basal and E2-induced activity were promoter dependent. iSp1, iSp3, and iSp4 also significantly inhibited hormonal induction of E2F1, CAD, and RARα mRNA levels; however, the enhanced inhibitory effects of the latter two small inhibitory RNAs suggest that Sp3 and Sp4 play a major role in estrogen receptor α/Sp-mediated gene expression in MCF-7 cells.

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